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本文引用的文献

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BDNF attenuates hippocampal LTD via activation of phospholipase C: implications for a vertical shift in the frequency-response curve of synaptic plasticity.脑源性神经营养因子通过激活磷脂酶C减弱海马长时程抑制：对突触可塑性频率-反应曲线垂直移位的影响
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A unified model of NMDA receptor-dependent bidirectional synaptic plasticity.NMDA受体依赖性双向突触可塑性的统一模型。
Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10831-6. doi: 10.1073/pnas.152343099. Epub 2002 Jul 22.
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Targeted disruption of RC3 reveals a calmodulin-based mechanism for regulating metaplasticity in the hippocampus.对RC3的靶向破坏揭示了一种基于钙调蛋白的调节海马体中可塑性的机制。
J Neurosci. 2002 Jul 1;22(13):5525-35. doi: 10.1523/JNEUROSCI.22-13-05525.2002.
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A biophysical model of bidirectional synaptic plasticity: dependence on AMPA and NMDA receptors.双向突触可塑性的生物物理模型：对AMPA和NMDA受体的依赖性。
Proc Natl Acad Sci U S A. 2001 Oct 23;98(22):12772-7. doi: 10.1073/pnas.201404598.
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Effect of transgenic overexpression of NR2B on NMDA receptor function and synaptic plasticity in visual cortex.NR2B转基因过表达对视觉皮层NMDA受体功能及突触可塑性的影响。
Neuropharmacology. 2001 Nov;41(6):762-70. doi: 10.1016/s0028-3908(01)00136-8.
6
Visual experience and deprivation bidirectionally modify the composition and function of NMDA receptors in visual cortex.视觉体验与视觉剥夺双向改变视皮层中NMDA受体的组成与功能。
Neuron. 2001 Jan;29(1):157-69. doi: 10.1016/s0896-6273(01)00187-8.
7
Synaptic activity modulates the induction of bidirectional synaptic changes in adult mouse hippocampus.突触活动调节成年小鼠海马体中双向突触变化的诱导。
J Neurosci. 2000 Apr 1;20(7):2451-8. doi: 10.1523/JNEUROSCI.20-07-02451.2000.
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Cumulative effects of glutamate microstimulation on Ca(2+) responses of CA1 hippocampal pyramidal neurons in slice.谷氨酸微刺激对脑片中海马CA1区锥体神经元Ca(2+)反应的累积效应。
J Neurophysiol. 2000 Jan;83(1):90-8. doi: 10.1152/jn.2000.83.1.90.
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Rapid, experience-dependent expression of synaptic NMDA receptors in visual cortex in vivo.视觉皮层中突触N-甲基-D-天冬氨酸受体在体内的快速、经验依赖性表达。
Nat Neurosci. 1999 Apr;2(4):352-7. doi: 10.1038/7263.
10
Inhibitory control of LTP and LTD: stability of synapse strength.长时程增强（LTP）和长时程抑制（LTD）的抑制性控制：突触强度的稳定性
J Neurophysiol. 1999 Apr;81(4):1559-66. doi: 10.1152/jn.1999.81.4.1559.

作为视觉皮层中可塑性变化基础的NMDA受体功能改变的证据。

Evidence for altered NMDA receptor function as a basis for metaplasticity in visual cortex.

作者信息

Philpot Benjamin D, Espinosa Juan S, Bear Mark F

机构信息

Howard Hughes Medical Institute and The Picower Center for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.

出版信息

J Neurosci. 2003 Jul 2;23(13):5583-8. doi: 10.1523/JNEUROSCI.23-13-05583.2003.

DOI:10.1523/JNEUROSCI.23-13-05583.2003
PMID:12843259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6741231/
Abstract

Sensory deprivation alters the properties of synaptic plasticity induced in the superficial layers of the visual cortex, facilitating long-term potentiation and reducing long-term depression (LTD) across a range of stimulation frequencies. Available data are compatible with either a downregulation of the mechanisms of LTD or an upregulation of NMDA receptor function in the visual cortex of dark-reared animals. Here, we provide evidence for enhanced NMDA receptor function by showing that deprivation produces a horizontal shift in the frequency-response function, decreasing LTD in response to 1 Hz stimulation, but increasing LTD in response to 0.5 Hz stimulation. In addition, we show that the effects of dark-rearing on the frequency dependence of LTD can be reversed acutely by partial NMDA receptor blockade. Finally, we show that an in vivo manipulation that rapidly downregulates NMDA receptor function in the visual cortex, brief light exposure, also rapidly reverses the effect of dark-rearing on LTD.

摘要

感觉剥夺会改变视觉皮层浅层诱导的突触可塑性特性，在一系列刺激频率下促进长时程增强并减少长时程抑制（LTD）。现有数据与暗饲养动物视觉皮层中LTD机制的下调或NMDA受体功能的上调均相符。在此，我们通过表明剥夺会使频率响应函数发生水平偏移来提供NMDA受体功能增强的证据：响应1Hz刺激时LTD减少，但响应0.5Hz刺激时LTD增加。此外，我们表明部分NMDA受体阻断可急性逆转暗饲养对LTD频率依赖性的影响。最后，我们表明一种能在体内快速下调视觉皮层中NMDA受体功能的操作——短暂光照，也能快速逆转暗饲养对LTD的影响。